Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype

Abstract Senescent cells are capable of expressing a myriad of inflammatory cytokines and this pro-inflammatory phenomenon is known as senescence-associated secretory phenotype (SASP). The contribution of this phenomenon in brain ischemia was scarce. A mouse model of transient focal cerebral ischemi...

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Autores principales:	Coral Torres-Querol, Pascual Torres, Noemí Vidal, Manel Portero-Otín, Gloria Arque, Francisco Purroy
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a33a8c378f5e40299a096dfba4c3232c
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spelling	oai:doaj.org-article:a33a8c378f5e40299a096dfba4c3232c2021-12-02T17:06:32ZAcute ischemic stroke triggers a cellular senescence-associated secretory phenotype10.1038/s41598-021-95344-52045-2322https://doaj.org/article/a33a8c378f5e40299a096dfba4c3232c2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-95344-5https://doaj.org/toc/2045-2322Abstract Senescent cells are capable of expressing a myriad of inflammatory cytokines and this pro-inflammatory phenomenon is known as senescence-associated secretory phenotype (SASP). The contribution of this phenomenon in brain ischemia was scarce. A mouse model of transient focal cerebral ischemia by compressing the distal middle cerebral artery (tMCAo) for 60 min was used. SASP, pro-inflammatory cytokines and cell cycle mRNAs levels were quantified at 30-min and 72 h post-surgery. Immunohistochemistry in paraffin embedded human brain slides and mouse brain tissue was performed. Our results showed an increase of both p16 and p21 mRNA restricted to the infarct area in the tMCAo brain. Moreover, there was an induction of Il6, Tnfa, Cxc11, and its receptor Cxcr2 mRNA pro-inflammatory cytokines with a high positive correlation with p16/p21 mRNA levels. The p16 was mainly shown in cytoplasm of neurons and cytoplasm/membrane of microglial cells. The p21 was observed in membrane of neurons and also it showed a mixed cytoplasmic and membranous pattern in the microglial cells. In a human stroke patient, an increase of P16 in the perimeter of the MCA infarct area was observed. These suggest a role of SASP in tMCAo mouse model and in human brain tissue. SASP potentially has a physiological role in acute ischemic stroke and neurological function loss.Coral Torres-QuerolPascual TorresNoemí VidalManel Portero-OtínGloria ArqueFrancisco PurroyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Coral Torres-Querol Pascual Torres Noemí Vidal Manel Portero-Otín Gloria Arque Francisco Purroy Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
description	Abstract Senescent cells are capable of expressing a myriad of inflammatory cytokines and this pro-inflammatory phenomenon is known as senescence-associated secretory phenotype (SASP). The contribution of this phenomenon in brain ischemia was scarce. A mouse model of transient focal cerebral ischemia by compressing the distal middle cerebral artery (tMCAo) for 60 min was used. SASP, pro-inflammatory cytokines and cell cycle mRNAs levels were quantified at 30-min and 72 h post-surgery. Immunohistochemistry in paraffin embedded human brain slides and mouse brain tissue was performed. Our results showed an increase of both p16 and p21 mRNA restricted to the infarct area in the tMCAo brain. Moreover, there was an induction of Il6, Tnfa, Cxc11, and its receptor Cxcr2 mRNA pro-inflammatory cytokines with a high positive correlation with p16/p21 mRNA levels. The p16 was mainly shown in cytoplasm of neurons and cytoplasm/membrane of microglial cells. The p21 was observed in membrane of neurons and also it showed a mixed cytoplasmic and membranous pattern in the microglial cells. In a human stroke patient, an increase of P16 in the perimeter of the MCA infarct area was observed. These suggest a role of SASP in tMCAo mouse model and in human brain tissue. SASP potentially has a physiological role in acute ischemic stroke and neurological function loss.
format	article
author	Coral Torres-Querol Pascual Torres Noemí Vidal Manel Portero-Otín Gloria Arque Francisco Purroy
author_facet	Coral Torres-Querol Pascual Torres Noemí Vidal Manel Portero-Otín Gloria Arque Francisco Purroy
author_sort	Coral Torres-Querol
title	Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
title_short	Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
title_full	Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
title_fullStr	Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
title_full_unstemmed	Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
title_sort	acute ischemic stroke triggers a cellular senescence-associated secretory phenotype
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a33a8c378f5e40299a096dfba4c3232c
work_keys_str_mv	AT coraltorresquerol acuteischemicstroketriggersacellularsenescenceassociatedsecretoryphenotype AT pascualtorres acuteischemicstroketriggersacellularsenescenceassociatedsecretoryphenotype AT noemividal acuteischemicstroketriggersacellularsenescenceassociatedsecretoryphenotype AT manelporterootin acuteischemicstroketriggersacellularsenescenceassociatedsecretoryphenotype AT gloriaarque acuteischemicstroketriggersacellularsenescenceassociatedsecretoryphenotype AT franciscopurroy acuteischemicstroketriggersacellularsenescenceassociatedsecretoryphenotype
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Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype

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